Seroatlas · Human Serome Atlas

CACNA1G

Voltage-dependent T-type calcium channel subunit alpha-1G

Also known as: CAC1G_HUMAN, Cav3.1, NBR13

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
O43497
Gene
CACNA1G
Ensembl
ENSG00000006283
Chromosome
17
Canonical length
2377 aa
Protein class
Disease related genes, FDA approved drug targets, Human disease related genes, Plasma proteins, Predicted membrane proteins, Voltage-gated ion channels
Subcellular location
Nucleoplasm,Nuclear bodies,Cytosol,Acrosome,Equatorial segment,Perinuclear theca

OverviewNCBI Gene

Voltage-sensitive calcium channels mediate the entry of calcium ions into excitable cells, and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division, and cell death. This gene encodes a T-type, low-voltage activated calcium channel. The T-type channels generate currents that are both transient, owing to fast inactivation, and tiny, owing to small conductance. T-type channels are thought to be involved in pacemaker activity, low-threshold calcium spikes, neuronal oscillations and resonance, and rebound burst firing. Many alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Sep 2011]

Canonical amino-acid sequenceUniProt

2377 residues, UniProt reviewed canonical sequence.

>O43497|CACNA1G
     1  MDEEEDGAGA EESGQPRSFM RLNDLSGAGG RPGPGSAEKD PGSADSEAEG LPYPALAPVV
    61  FFYLSQDSRP RSWCLRTVCN PWFERISMLV ILLNCVTLGM FRPCEDIACD SQRCRILQAF
   121  DDFIFAFFAV EMVVKMVALG IFGKKCYLGD TWNRLDFFIV IAGMLEYSLD LQNVSFSAVR
   181  TVRVLRPLRA INRVPSMRIL VTLLLDTLPM LGNVLLLCFF VFFIFGIVGV QLWAGLLRNR
   241  CFLPENFSLP LSVDLERYYQ TENEDESPFI CSQPRENGMR SCRSVPTLRG DGGGGPPCGL
   301  DYEAYNSSSN TTCVNWNQYY TNCSAGEHNP FKGAINFDNI GYAWIAIFQV ITLEGWVDIM
   361  YFVMDAHSFY NFIYFILLII VGSFFMINLC LVVIATQFSE TKQRESQLMR EQRVRFLSNA
   421  STLASFSEPG SCYEELLKYL VYILRKAARR LAQVSRAAGV RVGLLSSPAP LGGQETQPSS
   481  SCSRSHRRLS VHHLVHHHHH HHHHYHLGNG TLRAPRASPE IQDRDANGSR RLMLPPPSTP
   541  ALSGAPPGGA ESVHSFYHAD CHLEPVRCQA PPPRSPSEAS GRTVGSGKVY PTVHTSPPPE
   601  TLKEKALVEV AASSGPPTLT SLNIPPGPYS SMHKLLETQS TGACQSSCKI SSPCLKADSG
   661  ACGPDSCPYC ARAGAGEVEL ADREMPDSDS EAVYEFTQDA QHSDLRDPHS RRQRSLGPDA
   721  EPSSVLAFWR LICDTFRKIV DSKYFGRGIM IAILVNTLSM GIEYHEQPEE LTNALEISNI
   781  VFTSLFALEM LLKLLVYGPF GYIKNPYNIF DGVIVVISVW EIVGQQGGGL SVLRTFRLMR
   841  VLKLVRFLPA LQRQLVVLMK TMDNVATFCM LLMLFIFIFS ILGMHLFGCK FASERDGDTL
   901  PDRKNFDSLL WAIVTVFQIL TQEDWNKVLY NGMASTSSWA ALYFIALMTF GNYVLFNLLV
   961  AILVEGFQAE EISKREDASG QLSCIQLPVD SQGGDANKSE SEPDFFSPSL DGDGDRKKCL
  1021  ALVSLGEHPE LRKSLLPPLI IHTAATPMSL PKSTSTGLGE ALGPASRRTS SSGSAEPGAA
  1081  HEMKSPPSAR SSPHSPWSAA SSWTSRRSSR NSLGRAPSLK RRSPSGERRS LLSGEGQESQ
  1141  DEEESSEEER ASPAGSDHRH RGSLEREAKS SFDLPDTLQV PGLHRTASGR GSASEHQDCN
  1201  GKSASGRLAR ALRPDDPPLD GDDADDEGNL SKGERVRAWI RARLPACCLE RDSWSAYIFP
  1261  PQSRFRLLCH RIITHKMFDH VVLVIIFLNC ITIAMERPKI DPHSAERIFL TLSNYIFTAV
  1321  FLAEMTVKVV ALGWCFGEQA YLRSSWNVLD GLLVLISVID ILVSMVSDSG TKILGMLRVL
  1381  RLLRTLRPLR VISRAQGLKL VVETLMSSLK PIGNIVVICC AFFIIFGILG VQLFKGKFFV
  1441  CQGEDTRNIT NKSDCAEASY RWVRHKYNFD NLGQALMSLF VLASKDGWVD IMYDGLDAVG
  1501  VDQQPIMNHN PWMLLYFISF LLIVAFFVLN MFVGVVVENF HKCRQHQEEE EARRREEKRL
  1561  RRLEKKRRNL MLDDVIASGS SASAASEAQC KPYYSDYSRF RLLVHHLCTS HYLDLFITGV
  1621  IGLNVVTMAM EHYQQPQILD EALKICNYIF TVIFVLESVF KLVAFGFRRF FQDRWNQLDL
  1681  AIVLLSIMGI TLEEIEVNAS LPINPTIIRI MRVLRIARVL KLLKMAVGMR ALLDTVMQAL
  1741  PQVGNLGLLF MLLFFIFAAL GVELFGDLEC DETHPCEGLG RHATFRNFGM AFLTLFRVST
  1801  GDNWNGIMKD TLRDCDQEST CYNTVISPIY FVSFVLTAQF VLVNVVIAVL MKHLEESNKE
  1861  AKEEAELEAE LELEMKTLSP QPHSPLGSPF LWPGVEGPDS PDSPKPGALH PAAHARSASH
  1921  FSLEHPTDRQ LFDTISLLIQ GSLEWELKLM DELAGPGGQP SAFPSAPSLG GSDPQIPLAE
  1981  MEALSLTSEI VSEPSCSLAL TDDSLPDDMH TLLLSALESN MQPHPTELPG PDLLTVRKSG
  2041  VSRTHSLPND SYMCRHGSTA EGPLGHRGWG LPKAQSGSVL SVHSQPADTS YILQLPKDAP
  2101  HLLQPHSAPT WGTIPKLPPP GRSPLAQRPL RRQAAIRTDS LDVQGLGSRE DLLAEVSGPS
  2161  PPLARAYSFW GQSSTQAQQH SRSHSKISKH MTPPAPCPGP EPNWGKGPPE TRSSLELDTE
  2221  LSWISGDLLP PGGQEEPPSP RDLKKCYSVE AQSCQRRPTS WLDEQRRHSI AVSCLDSGSQ
  2281  PHLGTDPSNL GGQPLGGPGS RPKKKLSPPS ITIDPPESQG PRTPPSPGIC LRRRAPSSDS
  2341  KDPLASGPPD SMAASPSPKK DVLSLSGLSS DPADLDP

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against CACNA1G can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.

Antibody reachability
Cell surface
Secreted
No
Transmembrane segments
24
Mean surface accessibility (rSASA)
0.46
Highest tissue expression
19 nTPM

Expression across tissuesHPA

Tissue

  • cerebellum: 19 nTPM
  • cerebral cortex: 11 nTPM
  • cervix: 8.2 nTPM
  • retina: 8 nTPM
  • hypothalamus: 7.4 nTPM
  • ovary: 5.1 nTPM

Single-cell type

  • retinal bipolar cells: 188 nCPM
  • retinal amacrine cells: 132 nCPM
  • brain inhibitory neurons: 33 nCPM
  • oligodendrocyte progenitor cells: 26 nCPM
  • other brain neurons: 25 nCPM
  • brain excitatory neurons: 20 nCPM

Immune cell

  • neutrophil: 0.2 nTPM
  • gdT-cell: 0.1 nTPM
  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • intermediate monocyte: 0 nTPM

Brain region

  • thalamus: 101 nTPM
  • midbrain: 63 nTPM
  • cerebellum: 61 nTPM
  • spinal cord: 45 nTPM
  • cerebral cortex: 42 nTPM
  • hypothalamus: 39 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about CACNA1G.

Disease | AllUniProt

Conditions CACNA1G is implicated in, by any mechanism.

  • Spinocerebellar ataxia 42 (SCA42) MIM:616795
  • Spinocerebellar ataxia 42, early-onset, severe, with neurodevelopmental deficits (SCA42ND) MIM:618087

Disease | GeneticClinVar

30 pathogenic / likely-pathogenic of 1,504 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Disease | ImmuneIEDB

Conditions an epitope on CACNA1G was assayed in.

Genetic constraint and essentialitygnomAD · DepMap

Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.

gnomAD LOEUF (loss-of-function intolerance)
0.21
gnomAD pLI
1
gnomAD missense Z
4.64
DepMap mean gene effect
-0.25
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 2% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads CACNA1G as an antibody target. Whether an autoantibody or antibody against CACNA1G could matter depends on whether native CACNA1G is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

CACNA1G is annotated at the cell surface, where native CACNA1G is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.

Annotation status

The present source text does not explicitly label CACNA1G as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/CACNA1G. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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